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Vibrio parahaemolyticus

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Vibrio parahaemolyticus
SEM image of V. parahaemolyticus
Scientific classification
Kingdom:
Phylum:
Class:
Gamma Proteobacteria
Order:
Vibrionales
Family:
Genus:
Species:
V. parahaemolyticus
Binomial name
Vibrio parahaemolyticus
(Fujino et al. 1951)
Sakazaki et al. 1963

Vibrio parahaemolyticus is a curved, rod-shaped, Gram-negative bacterium found in brackish[1] saltwater, which, when ingested, causes gastrointestinal illness in humans.[1] V. parahaemolyticus is oxidase positive, facultatively aerobic, and does not form spores. Like other members of the genus Vibrio, this species is motile, with a single, polar flagellum.[2]

Pathogenesis

While infection can occur via the fecal-oral route, ingestion of bacteria in raw or undercooked seafood, usually oysters, is the predominant cause the acute gastroenteritis caused by V. parahaemolyticus.[3] Wound infections also occur, but are less common than seafood-borne disease. The disease mechanism of V. parahaemolyticus infections has not been fully elucidated.[4]

Clincal isolates usually possess a pathogenicity island (PAI) on the second chromosome. The PAI can be acquired via horizontal gene transfer and contains genes for several virulence factors. There are two fully sequenced variants of the Vibrio parahaemolyticus PAI with distinctly different lineages[5][6]. Each PAI variant contains a genetically-distinct Type III Secretion System (T3SS), which is capable of injecting virulence proteins into host cells to disrupt host cell functions or cause cell death via apoptosis. The two known T3SS variants on V. parahaemolyticus chromosome 2 are known as T3SS2α and T3SS2β. These variants correspond to the two known PAI variants. Aside from the T3SS, two genes encoding well-characterized virulence proteins are typically found on the PAI, the thermostable direct hemolysin gene (tdh) and/or the tdh-related hemolysin gene (trh). Strains possessing one or both of these hemolysins exhibit beta-hemolysis on blood agar plates. There seems to be a distinct correlation between presence of tdh, trh, and the two known T3SS variants: observations have shown T3SS2α correlating with tdh+/trh- strains, while T3SS2β correlates with tdh-/trh+ strains [7] .

Epidemiology

Outbreaks tend to be concentrated along coastal regions during the summer and early fall when higher water temperatures favor higher levels of bacteria. Seafood most often implicated includes squid, mackerel, tuna, sardines, crab, shrimp, and bivalves, such as oysters and clams. The incubation period of ~24 hours is followed by explosive, watery diarrhea accompanied by nausea, vomiting, abdominal cramps, and sometimes fever. Symptoms typically resolve within 72 hours, but can persist for up to 10 days in immunocompromised individuals. As the vast majority of cases of V. parahaemolyticus food infection are self-limiting, treatment is not typically necessary. In severe cases, fluid and electrolyte replacement is indicated.[2]

Additionally, swimming or working in affected areas can lead to infections of the eyes, ears,[8] or open cuts and wounds. Following Hurricane Katrina, 22 wounds were infected with Vibrio, three of which were caused by V. parahaemolyticus, and two of these led to death.

Hosts

Hosts of Vibrio parahaemolyticus include:

References

  1. ^ a b CDC Disease Info vibriop
  2. ^ a b Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9. {{cite book}}: |author= has generic name (help)CS1 maint: multiple names: authors list (link)
  3. ^ Finkelstein RA (1996). Cholera, Vibrio cholerae O1 and O139, and Other Pathogenic Vibrios. In: Barron's Medical Microbiology (Barron S et al., eds.) (4th ed.). Univ of Texas Medical Branch. (via NCBI Bookshelf) ISBN 0-9631172-1-1.
  4. ^ Baffone W, Casaroli A, Campana R, Citterio B, Vittoria E, Pierfelici L, Donelli G (2005). "'In vivo' studies on the pathophysiological mechanism of Vibrio parahaemolyticus TDH(+)-induced secretion". Microb Pathog. 38 (2–3): 133–7. doi:10.1016/j.micpath.2004.11.001. PMID 15748815.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Makino, Kozo (March 1, 2003). "Genome sequence of Vibrio parahaemolyticus: a pathogenic mechanism distinct from that of V. cholerae". The Lancet. 361: 743–479. PMID 19543642. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  6. ^ Okada, Natsumi (Feb 2009). "Identification and Characterization of a Novel Type III Secretion System in trh-positive Vibrio parahaemolyticus Strain TH3997 Reveal Genetic Lineage and Diversityt of Pathogenic Machinery beyond the Species Level". Infection and Immunity. 77 (2): 904–913. PMID 19075025. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)CS1 maint: date and year (link)
  7. ^ Noriea, Nicholas (September 2010). "Distribution of type III secretion systems in 'Vibrio parahaemolyticus from the northern Gulf of Mexico". Journal of Applied Microbiology. 109 (3): 953–962. PMID 20408916. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: date and year (link)
  8. ^ Penland RL, Boniuk M, Wilhelmus KR (2000). "Vibrio ocular infections on the U.S. Gulf Coast". Cornea. 19 (1): 26–9. doi:10.1097/00003226-200001000-00006. PMID 10632004.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ a b Kumazawa NH, Kato E, Takaba T, Yokota T. (August) 1988. Survival of Vibrio parahaemolyticus in two gastropod molluscs, Clithon retropictus and Nerita albicilla. Nippon Juigaku Zasshi. 50(4): 918-24.